Assistant Professor of Medicine
UPMC Montefiore Hospital - NW628
3459 Fifth Avenue
Pittsburgh, PA 15213

Phone: 412-802-8594
Fax: 412-692-2260
Email: petrovaa@upmc.edu
Assistant: Judy Nauman
Assistant Email: naumanja@upmc.edu

Paradoxical vocal Cord Dysfunction (VCD) is a hidden, yet common, usually unsuspected condition of throat closure, choking sensation, shortness of breath and  chronic cough. It that can strike any age, can cause sudden, severe episodes (attacks) of breathing difficulty, sometimes with wheezing (whistling or sighing sounds) &/or stridor (harsh, high pitched, ‘windy’ gasping sounds). In the Emergency Room (ER), VCD is usually misdiagnosed as being difficult asthma, anaphylaxis (severe, life threatening allergic reaction), or hysteria (all in one’s head). Patients will often state that their symptoms are triggered by exposure to strong scents (perfumes, cleaning chemicals, air fresheners …), exercise, etc. Other triggers include uncontrolled acid reflux and post-nasal drip.
Direct laryngoscopy is the most important test in making the diagnosis of VCD. Typically, one will see the partial or complete closing of vocal cords during the exam. The closing of vocal cords occurs during inspiration [breathing in/inhaling] or in both the inspiratory and expiratory [breathing out/exhaling] phases. However, the exam can be normal if a patient is not having symptoms and sometimes we will induce symptoms to confirm VCD diagnosis.
Treatment of VCD includes avoidance of environmental triggers, treatment of reflux, post-nasal drip and anxiety, breathing exercises and respiratory retraining with a speech therapist.

It is increasingly clear that the pathological event underlying most cases of asthma and allergic rhinitis (hay fever) is chronic allergic inflammation. A key event in  initiating allergen sensitization is the uptake, processing, and presentation of allergen by dendritic cells that are dedicated to this purpose. After contact with an antigen, these cells take up antigen and migrate within hours to regional lymph nodes where peptide fragments are presented to naïve T cell via MHC class II to the T cell receptor. Naïve T helper cells become activated and subsequently differentiate into Th2 type lymphocyte. The allergic response in asthma and allergic rhinitis is characterized by an immediate or early allergic response (EAR) and a late allergic response (LAR). EAR develops within 10 minutes of allergen exposure, reaching a maximum at 30 minutes, and resolving within 1-3 hours. It is now established that allergens initiate EAR through IgE-dependent mechanisms and the cell that initiates EAR is mast cell. Mast cells are present as resident cells in all tissues capable of mounting allergic responses. They bind IgE with high affinity to FcERI on their cell surface membranes. Mast cell activation occurs when allergen cross-links IgE-FcepsilonRI complexes on mast cells, which leads to degranulation of the mast cell and the release of preformed mediators including histamine, proteases and proteoglycans.

It also stimulates the mast cell to synthesize and generate newly generated mediators including leukotrienes (LTC4, LTD4, and LTE4), and prostanoids (PGD2, PGF2alpha, and TXA2).  Histamine, PGD2 and leukotrienes all have the ability to contract human bronchial smooth muscle. Mast cell also releases cytokines, growth factors and other mediators that attract T cells and inflammatory cells, especially eosinophils, into the airway tissue. This latter stage of inflammation represents LAR and it occurs several hours after EAR.  The influx of eosinophils and T lymphocytes results in the further
release of mediators. Most important cytokines of the LAR are IL-4, IL-5, IL-13, TNF α, and others. TH1 cells, which produce interferon-γ and tumour-necrosis factor, contribute to the allergic inflammation in certain situations.